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Transmigration of M1 and M 2 macrophages in pulmonary vessels following intratracheal bleomycin (834.7)
Author(s) -
Wang Ping,
Martin William
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.834.7
Subject(s) - bleomycin , pathology , macrophage , immunostaining , lung , inflammation , arginase , pulmonary fibrosis , chemistry , medicine , biology , microbiology and biotechnology , immunohistochemistry , immunology , fibrosis , in vitro , biochemistry , amino acid , chemotherapy , arginine
We have demonstrated macrophage transmigration in pulmonary vessels in murine lungs following bleomycin ( Am J Pathol . 2011 Jun; 178(6):2560‐72 ). Because there are two distinct phenotypes in macrophages, M1 and M2, we wanted to compare the difference between them in transmigration of pulmonary vessels. To address this, we intratracheally instilled bleomycin (3.33 U/kg) into female adult mice (C57BL/6J, n=8). Lungs were isolated at day 2‐21 after bleomycin and cryostat sectioned for immunostaining with iNOS and arginase I to identify M1 and M2 macrophages, respectively. We used ki67 as the marker of cell proliferation. We used confocal microscopy to image pulmonary vascular region covered from the lumen to the perivascular interstitium. We found that more macrophages expressed arginase I [6.7‐fold to iNOS, p<0.05, unpaired t ‐test], indicating that more M2 than M1 macrophages transmigrated in pulmonary vessels after bleomycin. Also, up to 20% M2 macrophages revealed ki67 expression (2‐fold to M1 macrophages, p<0.05) in arteriolar region, indicating higher local proliferation of M2 macrophages there. Our results provide direct evidence that primarily M2 macrophages transmigrated in pulmonary vessels. In addition, M2 exhibited more proliferation than M1 macrophages in pulmonary arterioles after bleomycin. This suggests an important role of M2 macrophages in bleomycin‐induced inflammation. (Funder: NIH) Grant Funding Source : NIH